首页> 外文期刊>In Vitro Cellular and Developmental Biology. Animal: Journal of the Tissues Culture Association >Insect cells and their potential as stabilization barriers for DNA of multiple and single nucleopolyhedroviruses against ultraviolet-B-simulated sunlight inactivation
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Insect cells and their potential as stabilization barriers for DNA of multiple and single nucleopolyhedroviruses against ultraviolet-B-simulated sunlight inactivation

机译:昆虫细胞及其作为多核和单核多角体病毒DNA抵抗紫外线B模拟日光灭活的稳定屏障的潜力

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A cell line from Trichoplusia ni (TN-CL1) infected with the Autographa californica multiple nucleopolyhedrovirus (AcMNPV-HPP) and a cell line from Helicoverpa zea (BCIRL-HZ-AM1) infected with the Helicoverpa zea single nucleopolyhedrovirus (HzSNPV/BrCL2) were subjected to ultraviolet-B (UV-B) irradiation at a predetermined level of exposure that would inactivate greater than 95% of the virus suspended in the liquid. The working hypothesis was that the homologous insect cells would utilize their inherent deoxyribonucleic acid (DNA) repair mechanism(s) to prevent, repair, or at least mitigate the damaging effects of UV-B light on viral DNA synthesis. We attempted to determine this by using infected cells that were subjected to UV-B irradiation at different postinoculation periods under two experimental conditions of exposure: (1) shielded, and (20 nonshielded. Of the two cell lines infected with their respective homologous viruses, the virus from TN-CL1 cells was the least sensitive to UV-B light because the extracellular virus (ECV) and occlusion body (OB) levels of virus-infected TN-CL1 cells were higher than those of the virus-infected BCIRL-HZ-AM1 cells. Production of ECV and OB from both cell lines was lower in the exposed, nonshielded treatment than in the exposed, shielded treatment. However, AcMNPV-HPP was produced in enough quantity to indicate that TN-CL1 might impart a level of protection to the virus against UV light.
机译:感染了加州白粉虱多核多角体病毒(AcMNPV-HPP)的Trichoplusia ni(TN-CL1)的细胞系和感染了Helicoverpa zea单核多角体病毒(HzSNPV / BrCL2)的Helicoverpa zea(BCIRL-HZ-AM1)的细胞系在预定的暴露水平下经受紫外线-B(UV-B)辐射,可使超过95%悬浮在液体中的病毒灭活。可行的假设是,同源昆虫细胞将利用其固有的脱氧核糖核酸(DNA)修复机制来预防,修复或至少减轻UV-B光对病毒DNA合成的破坏作用。我们尝试通过使用在两个接种后的不同暴露条件下在不同接种后阶段进行UV-B照射的感染细胞来确定这一点:(1)屏蔽的和(20个非屏蔽的。在两种细胞系中分别感染了各自的同源病毒,来自TN-CL1细胞的病毒对UV-B光的敏感度最低,因为被病毒感染的TN-CL1细胞的细胞外病毒(ECV)和遮挡体(OB)水平高于被病毒感染的BCIRL-HZ -AM1细胞:在暴露的非屏蔽处理中,两种细胞系产生的ECV和OB均比在暴露的非屏蔽处理中低,但是AcMNPV-HPP的生成量足以表明TN-CL1可能赋予保护病毒免受紫外线侵害。

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